Influence of central command and muscle afferent activation on anterior cerebral artery blood velocity responses to calf exercise in humans

2009 ◽  
Vol 107 (4) ◽  
pp. 1113-1120 ◽  
Author(s):  
Lauro C. Vianna ◽  
Claudio Gil S. Araújo ◽  
James P. Fisher
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Anterior Cerebral Artery ◽  
Muscle Afferents ◽  
Blood Velocity ◽  
Calf Muscle ◽  
Central Command ◽  
Muscle Stretch ◽  
Calf Exercise ◽  
Exercise Induced

The purpose of the present study was to determine the relative importance of peripheral feedback from mechanically (mechanoreflex) and metabolically (metaboreflex) sensitive muscle afferents and central signals arising from higher centers (central command) to the exercise-induced increases in regional cerebral perfusion. To accomplish this, anterior cerebral artery (ACA) mean blood velocity ( Vmean) responses were assessed during sustained and rhythmic passive calf muscle stretch (mechanoreflex), volitional calf exercise (mechanoreflex, metaboreflex, and central command), and electrically stimulated calf exercise (mechanoreflex and metaboreflex but no central command) at 35% of maximum voluntary contraction ( n = 16). In addition, a period of postexercise muscle ischemia (PEMI) was used to isolate the metaboreflex. Blood pressure, cardiac output, and the end-tidal partial pressure of carbon dioxide (PetCO2) were also measured. ACA Vmean was unchanged from rest during either sustained or rhythmic calf muscle stretch ( P > 0.05). However, ACA Vmean was increased from rest during both isometric (+15 ± 1%) and rhythmic (+15 ± 2%, voluntary exercise P < 0.05) but remained unchanged during stimulated exercise ( P > 0.05). Isometric and rhythmic exercise-induced increases in blood pressure and cardiac output were similar during voluntary and stimulated exercise ( P > 0.05 between conditions). Blood pressure remained elevated during PEMI after all exercise conditions ( P < 0.05 vs. rest), whereas cardiac output and ACA Vmean were not different from rest ( P > 0.05). PetCO2 was unchanged from rest throughout. These data suggest that selective activation of skeletal muscle afferents (i.e., stretch, PEMI, or stimulated exercise) does not increase ACA Vmean and that increases in ACA Vmean during volitional contractions of an exercising calf muscle are dependent on the presence of central command.

scholarly journals Aging alters muscle reflex control of autonomic cardiovascular responses to rhythmic contractions in humans

2015 ◽  
Vol 309 (9) ◽  
pp. H1479-H1489 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Joshua C. Weavil ◽  
Massimo Venturelli ◽  
Matthew J. Rossman ◽  
Benjamin S. Gmelch ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiovascular Response ◽  
Knee Extensor ◽  
Cardiovascular Responses ◽  
Muscle Afferents ◽  
Group Iii ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Exercise Induced ◽  
The Impact

We investigated the influence of aging on the group III/IV muscle afferents in the exercise pressor reflex-mediated cardiovascular response to rhythmic exercise. Nine old (OLD; 68 ± 2 yr) and nine young (YNG; 24 ± 2 yr) males performed single-leg knee extensor exercise (15 W, 30 W, 80% max) under control conditions and with lumbar intrathecal fentanyl impairing feedback from group III/IV leg muscle afferents. Mean arterial pressure (MAP), cardiac output, leg blood flow (QL), systemic (SVC) and leg vascular conductance (LVC) were continuously determined. With no hemodynamic effect at rest, fentanyl blockade during exercise attenuated both cardiac output and QL ∼17% in YNG, while the decrease in cardiac output in OLD (∼5%) was significantly smaller with no impact on QL ( P = 0.8). Therefore, in the face of similar significant ∼7% reduction in MAP during exercise with fentanyl blockade in both groups, LVC significantly increased ∼11% in OLD, but decreased ∼8% in YNG. The opposing direction of change was reflected in SVC with a significant ∼5% increase in OLD and a ∼12% decrease in YNG. Thus while cardiac output seems to account for the majority of group III/IV-mediated MAP responses in YNG, the impact of neural feedback on the heart may decrease with age and alterations in SVC become more prominent in mediating the similar exercise pressor reflex in OLD. Interestingly, in terms of peripheral hemodynamics, while group III/IV-mediated feedback plays a clear role in increasing LVC during exercise in the YNG, these afferents seem to actually reduce LVC in OLD. These peripheral findings may help explain the limited exercise-induced peripheral vasodilation often associated with aging.

scholarly journals Cardiovascular Reflexes Activity and Their Interaction during Exercise

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Antonio Crisafulli ◽  
Elisabetta Marongiu ◽  
Shigehiko Ogoh
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Oxygen Supply ◽  
Dynamic Exercise ◽  
Cardiovascular Reflexes ◽  
Arterial Blood ◽  
Functional Sympatholysis ◽  
Exercise Induced ◽  
By Products

Cardiac output and arterial blood pressure increase during dynamic exercise notwithstanding the exercise-induced vasodilation due to functional sympatholysis. These cardiovascular adjustments are regulated in part by neural reflexes which operate to guarantee adequate oxygen supply and by-products washout of the exercising muscles. Moreover, they maintain adequate perfusion of the vital organs and prevent excessive increments in blood pressure. In this review, we briefly summarize neural reflexes operating during dynamic exercise with particular emphasis on their interaction.

Effects of midodrine on exercise-induced hypotension and blood pressure recovery in autonomic failure

2004 ◽  
Vol 97 (5) ◽  
pp. 1978-1984 ◽  
Author(s):  
William G. Schrage ◽  
John H. Eisenach ◽  
Frank A. Dinenno ◽  
Shelly K. Roberts ◽  
Christopher P. Johnson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Autonomic Failure ◽  
Peripheral Resistance ◽  
Venous Occlusion ◽  
Open Circuit ◽  
Induced Hypotension ◽  
Calf Exercise ◽  
Exercise Induced ◽  
Similar Peak

We tested the hypothesis that the oral α1-adrenergic agonist, midodrine, would limit the fall in arterial pressure observed during exercise in patients with pure autonomic failure (PAF). Fourteen subjects with PAF underwent a stand test, incremental supine cycling exercise (25, 50, and 75 W), and ischemic calf exercise, before (control) and 1 h after ingesting 10 mg midodrine. Heart rate (ECG), beat-to-beat blood pressure (MAP, arterial catheter), cardiac output (Q̇, open-circuit acetylene breathing), forearm blood flow (FBF, Doppler ultrasound), and calf blood flow (CBF, venous occlusion plethysmography) were measured. The fall in MAP after standing for 2 min was similar (∼60 mmHg; P = 0.62). Supine MAP immediately before cycling was greater after midodrine (124 ± 6 vs 117 ± 6 mmHg; P < 0.03), but cycling caused a workload-dependent hypotension ( P < 0.001), whereas increases in Q̇ were modest but similar. Midodrine increased MAP and total peripheral resistance (TPR) during exercise ( P < 0.04), but the exercise-induced fall in MAP and TPR were similar during control and midodrine ( P = 0.27 and 0.14). FBF during cycling was not significantly reduced by midodrine ( P > 0.2). By contrast, recovery of MAP after cycling was faster ( P < 0.04) after midodrine (∼25 mmHg higher after 5 min). Ischemic calf exercise evoked similar peak CBF in both trials, but midodrine reduced the hyperemic response over 5 min of recovery ( P < 0.02). We conclude midodrine improves blood pressure and TPR during exercise and dramatically improves the recovery of MAP after exercise.

scholarly journals The cardiac output from blood pressure algorithms trial*

2009 ◽  
Vol 37 (1) ◽  
pp. 72-80 ◽  
Author(s):  
James X. Sun ◽  
Andrew T. Reisner ◽  
Mohammed Saeed ◽  
Thomas Heldt ◽  
Roger G. Mark
Keyword(s):  
Blood Pressure ◽  
Cardiac Output

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

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